Acute Coronary Syndromes Flashcards

1
Q

Atherosclerotic Plaque Formation

A
  1. Endothelial dysfunction and high circulation LDL in lumen deposit in tunica intima and oxidise
  2. Endothelial cells expose WBC receptors and Reactive oxygen species
    Adhesion of WBC - monocytes and T-helper cells to move into tunica intima
  3. Become macrophages and take up LDL to become foam cells. Release Chemokines to attract more macrophages.

4 . These release IGF-1 causing migration of smooth muscle cells from tunica media to tunica intima. Increased SMC proliferation leads to more synthesis of collagen – leading to hardening.

  1. Foam cells die and spill lipid content leading to attraction of neutrophils and proinflammatory reactive o2 species.
  2. Plaque rupture.
    Coagulation happens to stop plaque spilling into lumen leading to thrombus formation.
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1
Q

Acute Coronary Syndromes

A

Result of a thrombus from an atherosclerotic plaque blocking a coronary artery.

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2
Q

Thrombus Formation

A

Virchows Triad: Hypercoagulability, Endothelial injury,
Vascular damage

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3
Q

Troponin

A

Rise in troponin due to myocardial ischaemia (released from ischaemic muscle tissue).

A high or rising troponin indicates a NSTEMI.

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4
Q

Troponin Indications

A

CKD
Sepsis
Myocarditis
Aortic Dissection
PE or Stroke
MI

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5
Q

Presentation of ACS

A

Pain - radiating to jaw or arms
N+V
Sweating and Clamminess
Feeling of impending doom
SOB
Palpitations

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6
Q

Ix for ACS

A

Baseline bloods : FBC, U+E, LFT, Lipids and glucose
Troponin
ECG

Others:
Cxr - pulmonary oedema or other causes of chest pain.

Echocardiogram - assessing functional damage (specifically LV)

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7
Q

Classification ACS

A

Angina: Symptoms upon exertion and settle at rest.

Unstable Angina:
Symptoms at rest with no further damage

NSTEMI:
Symptoms at rest with no or partial infarction.

STEMI:
Symptoms at rest with complete occlusion / infarction of coronary tissue.

Silent MI : No symptoms or the typical chest pain during an ACS episode. Diabetes patients are at most risk.

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8
Q

Investigation findings for unstable angina

A

Normal ECG or ST depression or T wave inversion.
Troponin will be normal

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9
Q

Investigation findings for NSTEMI

A

ECG - ST depression and T wave inversion
Ix - Troponin - baseline, 3 hours after symptoms.

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10
Q

Investigation findings for STEMI

A

ECG - ST Elevation and new left BBB.
Troponin is not required (often done) due to ECG findings consistent with STEMI.

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11
Q

Type 1 MI

A

Traditional MI due to an acute coronary event

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12
Q

Type 2 MI

A

Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)

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13
Q

Type 3 MI

A

Sudden cardiac death or cardiac arrest suggestive of an ischaemic event

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14
Q

Type 4 MI

A

MI associated with procedures such as PCI, coronary stenting and CABG

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15
Q

Initial Treatment ACS

A

MONA:
Morphine // any other pain relief only if pt is in pain
Oxygen - Only if low O2
Nitrates - GTN
Aspirin 300mg

16
Q

NSTEMI Treatment

A

300mg Aspirin and continue indefinitely unless CI

Offer fondaparinux unless high bleeding risk or immediate angiography.

Risk assessment - GRACE - for 6 month mortality risk

Low risk - Conservative management - ticagrelor with aspirin or clopidogrel if high bleeding risk.

Intermediate or high risk - PCI within 72 hours if stable. Ticagrelor with aspirin.

17
Q

STEMI Treatment

A

300mg Aspirin and continue indefinitely unless CI
Referral for Reperfusion Therapy (Primary PCI or fibrinolysis)

Within 12 hours and PCI within 120 min - Angiography with follow on Primary PCI

Within 12 hours and PCI not within 120 min - Fibrinolysis

Neither - Ticagrelor with aspirin (unless bleeding risk then switch to aspirin and clopidogrel) with follow up.

18
Q

PCI

A

Primary cutaneous intervention

Opening of blocked arteries to improve blood flow to the tissue. Thin catheter inserted into the artery guided by X Ray via femoral or radial artery.

19
Q

Fibrinolysis

A

Fibrinolytic drugs when PCI not completed in time - dissolves the fibrin clots - alteplase, reteplase and tenecteplase. High bleeding risk and inc risk of ICH.

20
Q

Secondary prevention of ACS

A

BADS WEEDS
Assessment appointment within 10 days of discharge

Drug Therapy - BADS
- Beta Blocker in reduced LVef or up to 12 months
- ACE inhibitor
- Dual antiplatelet therapy for up to 12 months - Clopidogrel if had a PCI, Aspirin alone if no PCI.
- Statins

Lifestyle - WEEDS
Weight
Exercise
Ethanol (alcohol)
Diet / Drugs
Smoking

21
Q

Complications ACS

A

DREAD
D - Death
R - Rupture of heart septum
E - Edema (HF)
A - Arrhythmia or Aneurysm
D - Dressler Syndrome

22
Q

Dressler Syndrome

A

(Post MI Pericarditis)

2-3 weeks after acute MI

Localised immune response that results in inflammation in pericardium

Pleuritic chest pain, low grade fever and a pericardial rub.

23
Q

Ix Dressler Syndrome

A

ECG - Global ST elevation and T wave Inversion
Echo - pericardial effusion
Raised inflammatory markers - CRP and ESR

24
Management Dressler Syndrome
Management - NSAIDs and in some steroids (prednisolone). Pericardiocentesis may be required to remove excess fluid.
25
Non-Modifiable Risk Factors
Increasing age Male gender Family history
26
Modifiable Risk Factors
Smoking Diabetes mellitus Hypertension Hypercholesterolaemia Obesity